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MHD I > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Where are micrococcus and Staphyloccus commonly recovered from?

A

From the environment or as commensals inhabiting skin and mucus membranes

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2
Q

Key characteristics of Staphylococci

A
  1. ​Gram-positive
  2. ​Grape-like clusters
  3. Non-motile
  4. Non-spore-forming
  5. Catalase positive
  6. Usually facultative anaerobes
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3
Q

Staph Aureus cluster pattern and color

A
  • Grape like clusters
  • Creme (or golden brown)
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4
Q

Staph Aureus Habitat

A
  • External environment
  • Skin and mucous membranes
  • 20-40% in the anterior nares
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5
Q

Factors predisposing to serious infection with Staph Aureus (8)

A
  1. Defects in leukocyte chemotaxis
  2. Defects in opsonization by antibodies
  3. Defects in intracellular killing of bacteria due to inability to activate the membrane bound oxidase system
  4. Skin injuries
  5. Presence of foreign bodies
  6. Infection with other agents (e.g. viruses)
  7. Chronic underlying disease
  8. Use of antibiotics to which S. aureus is not susceptible
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6
Q

Signs of serious infection of Staph aureus (5) + examples

A
  1. Pyoderma
  2. Furuncle (boils)
  3. Carbuncle
  4. Toxin-Mediated Infections
    • Scalded skin syndrome
    • Toxic-shock syndrome
    • Food poisoning
  5. Disseminated Infections
    • Osteomyelitis
    • Endocarditis
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7
Q

Staph Aureus Virulence Factors

A
  1. Capsules
  2. Protein A
  3. Panton-Valentine Leukocidin (PVL) (enzymes that alters cation permeability leading to white cell destruction)
  4. Coagulase
  5. Hemolysins (alpha, beta, delta, gamma)
  6. Toxins (exfoliatins, enterotoxins, enzymes)
  7. Superantigens (TSST-1)
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8
Q

Delta-hemolysin

A

Virulence factor of Staph Aureus.

Produced by 97% of S. aureus. Acts as surfactant that disrupts the cell membrane, interacts with the membrane to form channels that increase the size resulting in leakage of cellular contents.

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9
Q

What causes scalded skin syndrome?

A

Staph Aureus have exfoliatins/ epidermolytic toxins that dissolve the mucopolysaccharide matrix of epidermis, causing separation of skin layers

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10
Q

What is responsible for the clinical features of staphylococcal food poisoning?

A

Entertoxins

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11
Q

Superantigens (+ types (3)+ biological characteristics in common (4))

A

Group of toxins known as pyrogenic toxin superantigens. These include:

  1. Toxic shock syndrome toxin-1 (TSST-1)
  2. Streptococcal pyrogenic exotoxins (SPE)
  3. Streptococcal superantigens

All possess 3 biologic characteristics:

  1. Pyrogenicity
  2. Superantigenicity
  3. Enhance lethal effects of minute amounts of endotoxin
  4. Induce polyclonal T-cell proliferation
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12
Q

Key facts about Staph. Epidermis (Frequency of isolation? What is it associated with? What is virulence related to? Role of Biofilm?)

Coagulase + or - ?

A
  • Most frequently isolated clincally signative ​coagulase-negative staphylococci
  • Associated with infections of indwelling devices
  • Virulence related to production of extracellular slime that promotes adherence​ to surgace of forign bodies (forming biofilm)
  • ​Biofilm plays important role in protection from antimicrobial angents, therefore FULL REMOVAL OF INDWELLING DEVICE IS NEEDED FOR FULL INFECTION REMOVAL.
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13
Q

Staphylococcus saphrophyticus

(What does it cause? What is its identification based upon?)

A
  • Cause of acute urinary tract infection in young women
  • 2nd most common cause of uncomplicated cystitis among women of college and child-bearing age
  • Identification based on negative coagulase and resistance to novobiocin
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14
Q

Staphylococcus Lugdunensis (key features + what is unique about it?)

A
  1. Colonizes human inguinal area
  2. Causes wide variety of human infections
  3. Only species that is both ​PYR and Orthine positive
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15
Q

In hospitals, what is the most important reservoir of MRSA? Who can serve as the link between these populations?

A

Colonized or infect patients. Hospital personnel can serve as a link for transmission between colonized or infected patients.

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16
Q

The (6) settings associated with CA-MRSA

A
  1. Sports participants
  2. Correctional facilities
  3. Military recruits
  4. Daycare and other institutional centers
  5. Newborn nurseries and other healthcare settings
  6. Men who have sex with men (MSM)
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17
Q

Key gene of MRSA

A

The mecA Gene

It encodes for altered “penicillin-binding protein 2a”. Has decreased binding affinity for B-lactam antibiotics (e.g. penicillin). This is what makes them resistant.

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18
Q

Disease Symptoms in which MRSA should be considered a differential diagnosis.

A
  1. Skin and soft tissue infections (boils, spider bites, and cellulitis)
  2. Sepsis Syndrome
  3. Osteomyelitis
  4. ​Necrotizing pneumonia
  5. Septic arthritis
  6. Necrotizing fasciitis
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19
Q

MRSA Infection Prevention Methods

A
  1. Active Surveillance (test all patients)
  2. Contact precautions
  3. Cleaning
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20
Q

Staphylococci vs Streptococci (Catalase, physical arrangment, media, temperature for growth, prefered atmosphere?)

A

Staphylococci:

  • Catalase positive
  • Cocci in clusters
  • Grows in minimal media
  • Grows best at 35-37 C
  • Aerobic preference

​Streptococci:

  • ​Catalase negative
  • ​Cocci in pairs/chains
  • ​Requires complex media
  • ​Grows best at 35-37 (same as staph)
  • Prefers anaerobic/ CO2 atmosphere
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21
Q

Catalase

A

Common enzyme found in nearly all living organisms exposed to oxygen. IT catalyzes the decomposition of hydrogen peroxide to water and oxygen. Important in protecting the cell from ROS’s

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22
Q

The 3 classifications of Streptococci Hemolysis

A
  1. Beta​- complete hemolysis
  2. Alpha​- incomplete hemolysis
  3. Gamma​- no hemolysis
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23
Q

What bacteria is associated with Strep Lancefield Group A?

A

Streptococcus pyogenes

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24
Q

What bacteria is associated with Strep Lancefield Group B

A

Streptococcus agalactiae

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25
Q

The (6) clinical manifestations of Streptococcus pyogenes infection

A
  1. Acute Pharyngitis
  2. Impetigo
  3. Erysipelas
  4. Scarlet Fever
  5. Necrotizing Fasciitis
  6. Toxic Shock-like Syndrome
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26
Q

Impetigo (characteristics + age of association)

A
  • Associated with S. pyogenes Infections
  • Pustule with yellow crust which appears on face or extremities
  • 2-5 y/o children
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27
Q

Erysipelas

A
  • Spreading erythema with well demarcated edge on the legs (historically on the face)
  • Associated with S. pyogenes infections
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28
Q

Scarlet Fever is a complication of _______ _______.

It is caused by ________ ________

Signs and Symptoms?

A
  1. Complication of streptococcal pharyngitis
  2. Casued by erythrogenic exotoxin
  3. Rash
  4. ​Blanches, Sore throat, Bright Red “Strawberry” Tongue
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29
Q

Necrotizing Fasciitis

A

Strep infection that occurs deep in the subcutaneous tissues and leads to extensive destruction of the muscle and fat (flesh-eating)

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30
Q

What bacteria is Toxic Shock-like Syndrome Associated with?

A

Usually group A strep

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31
Q

Puerperal Sepsis?

A
  • Seen in women following delivery or abortion
  • Organisms colonizing genital tract or from OB personell invade upper GU tract leading to toxic shockk-like syndrome, nec. fasciitis, etc.
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32
Q

Post-Streptococcal Sequelae (2)

A
  1. Rheumatic Fever​: Inflammatory disease 1-5 weeks after strep pharyngitis with reoccuring attacks. Characteristic cardiac lesions which can later lead to possible endocarditis. Associated with fever, carditis and polyarthritis.
  2. ​Acute Glomerulonephritis​: Occurs after skin/respiratory infection. Edema, hypertension, hematuria and proteinuria. Immune complexes often deposited in glomeruli.
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33
Q

Virulence Factors of Group A Streptococci (4)

A
  1. Adherence (capsular polysaccharide)
  2. Invasion of epithelial cells
  3. Avoidance of opsonization and phagocytosis
  4. Production of toxins/enzymes (3 distinct heat labile toxins called superantigens)
    • Responsible for rash in scarlet fever
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34
Q

Treatment of S. pyogenes

A
  • Penicillin/ ampicillin/ amoxacillin (drug of choice- no resistance worldwide​)
  • ​Cephalosporins
  • ​Erythromycin
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35
Q

Streptococcus agalactiae

Role in neonatal disease and how is it prevented

A

GBS

Plays role in neonatal pneumonia, sepsis and meningitis. Maternal colonization of vagina or rectum exposes baby at delivery.

​Prevention​: Cultures should be taken at 35 to 37 weeks and penicillin/ampicillin is given prophylatically

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36
Q

Limitation of Group A Rapid Test

A

It has a decreased sensitivity, which makes it less accurate. You must follow it up with the culture to get the final word.

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37
Q

Isolation of a bovis group from the blood is associated with…

A

…patients with carcinoma of the colon

(Cow Cancer Colon)

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38
Q

Species included in the Strep Milleri Group (3) and what is their role?

A
  1. S. anginosus
  2. S. constellatus
  3. S. intermedius

Commensals, but can cause deep-seated pyogenic infections

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39
Q

Species included in Nutritionally Deficient Streptococci

A
  1. Abiotrophia
  2. Granulicatella
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40
Q

Identify the key morphologic/ virulent factors of S.pneumoniae

A

Structural characteristics: Gram positive; polysaccharide capsule; bile-susceptible; IgA protease

​

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41
Q

Most common cause of bacterial meningitis in the U.S.?

Highest rate of meningitis among children younger than 2 years?

A

Invasive Pneumococcal Disease caused by s. pneumoniae. (for both questions)

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42
Q

Phenotype of S. pneumoniae as determined in the lab

A
  1. Gram +
  2. Lancet-shaped cocci (elongated w/ slightly pointed curvature)
  3. Usually diplococci (but not always)
  4. Catalase negative
  5. BIle soluble
  6. Inhibited by Optochin
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43
Q

When cultured on blood agar, S. pneumoniae shows what type of hemolysis?

A

It is alpha hemolytic

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44
Q

The 2 main species of Enterococcus and their relationship to penicillin/ ampicillin

What is their general resistance?

A
  1. ​E. faecalis ​(susceptible to pen/amp)
  2. E. faecium ​(resistant to pen/amp)

Both are inherently reisistant to many commonly used antibiotics

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45
Q

The 3 most common infections caused by enterococci

What infection occurs rarely?

A
  1. Mixed bacterial wound infections
  2. Sepsis
  3. Endocarditis
  4. RARELY meningitis
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46
Q

Enterococci are intrinsically resistant to…

A

…all cephalosporins, aminoglycosides, and trimethoprim-sulfa

(CATs)

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47
Q

Basic Enterococcus Characterisitics (4)

A
  1. Gram positive cocci in pairs and short chains
  2. Alpha, beta or gamma hemolytic
  3. Group D antigen pos.
  4. PYR pos.
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48
Q

What are the two pathological species of Neisseria?

A
  1. Meningitidis
  2. Gonorrhoeae
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49
Q

General characteristics of enterobacteriaceae

A
  1. Gram negative rods
  2. Indigenous flora of GI tract
  3. Colonize resp. tract of hospitalized patients
  4. Grow rapidly aerobically/ anaerobically
  5. Simple growth requirements
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50
Q

Key endotoxin affliated with enterobacteriaceae?

A

LPS

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51
Q

What part of LPS is responsible for its toxicity?

A

Lipid A– the inner most region of LPS. Responsbile for the endotoxin abilities of enterobacteriaceae. The fragments of this are responsible for shock.

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52
Q

The 4 unwavering biochemical characteristics shared by all enterobacteriaceae.

A
  1. Faculatative Gram-Neg rods
  2. Ferment glucose
  3. Reduce nitrate to nitrite
  4. Oxidase negative
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53
Q

The most important species of Escherichieae

A

E. coli

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54
Q

E. coli habitat

A

Intestines of humans and animals (no where in the external enivronment)

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55
Q

Clinical Syndromes associated with E. Coli (6)

A
  1. Gram negative sepsis
  2. UTI’s (80% of community acquired UTI’s)
  3. Wound infections
  4. Pneumoniain IC hospitalized patients
  5. Meningitis in neonates
  6. Gastroenteritis
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56
Q

Name the five groups of E. coli that can cause gastroenteritis and the signs and symptoms of diarrheal disease that is produced by each group .

A
  1. Enterotoxigenic E. coli (ETEC)​- profuse watery diarrhea (traveler’s)
  2. ​Enteropathogenic E. coli​​ (EPEC)​- Infants. Mucusy diarrhea, but NO gross blood
  3. Enteroinvasive E. coli​​ (EIEC)​- Blood, mucus and many leukocytes in stool
  4. Entero-Hemorrhagic E. coli (EHEC)​- Bloody diarrhea w/o WBCs. Produce shiga-like toxin (STEC)
  5. ​Enteroaggregative E. coli​ (EAggEC)- Watery diarrhea with blood and mucus
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57
Q

Shiga Toxin (STEC) is associated with what type of E. coli

A

Entero-Hemorrhagic E. coli (EHEC) –> Primarily caused by E. coli O157:H7

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58
Q

Resevoir and Transmission of E. coli O157

A
  • Reservoir: Healthy Dairy Cattle
  • Tranmission: Food (usually ground beef), water, or direct contact with an infected patient

STEC is shed in the feces of cattle, sheep, deer, and other ruminants

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59
Q

Triad of symptoms for ​Hemolytic Uremic Syndrome

A
  1. acute renal failure
  2. thrombocytopenia
  3. hemolytic anemia
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60
Q

​Laboratory Diagnosis of Disease caused by Shiga-toxin (Timing, type and transport of specimen?)

What is used for the actual diagnosis?

A
  • ​Timing: ​Specimens are best collected early, when organism load is higher and before antibiotics
  • Type:​ Whole stool is preferred
  • Transport:​ As soon as possible. Refrigerate if more than 1-2 hours

Antigen detection or FilmArray GI Panel (Multiplex PCR) is used for the final detection.

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61
Q

Treatment of STEC diseases (how is the diarrhea treated? antibiotics or no? antimoltility drugs or no?)

A

DIarrhea:​ Oral rehydration; HUS/ renal failuremanaged by dialysis; NO ANTIBIOTICS OR ANTIMOTILITY AGENTS (can increase HUS risk)

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62
Q

Strep Pneumo is the #1 cause for what (4) diseases?

A

MOPS

  1. Menengitis
  2. Otitis media
  3. Pneumonia
  4. Sinusitis
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63
Q

Shigella is very similar to E.coli but has some differences. What are the key id features of Shigella which sepearate it from E.coli? (3)

A
  1. Non-lactose fermenter
  2. Non gas producer
  3. Nonmotile
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64
Q

What are the modes for shigella transmission?

A

Person to person via fecal oral route

Usually via contaminated…

  1. water
  2. 5 F’s (food, flies, fingers, fomites and feces)
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65
Q

Who’s at highest risk for Shigella Transmission? (3 groups)

A
  1. Young children in day care center, nurseries, or custodial institutions
  2. Siblings/parents of these children
  3. Male homosexuals
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66
Q

Clinical manifestation of Shigella

A

Bacillary Dysentery

  • ​Signs and Symptoms: Abdominal cramps; tenesmus (urge to poop but there is none); pus and blood in stool; Fecal leukocytes are present
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67
Q

What is the important species of Edwardsielleae?

A

Edwardseilla tarda (E. tarda)

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68
Q

Habitat for E. tarda (3)

A

Cold blooded vertebrates; fresh water; catfish

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69
Q

Main clinical syndromes associated with E. tarda (2)

What is it sometimes mistaken for?

A
  1. ​Acute, self-limiting Gastroenteritis ​with watery diarrhea. Can develop to typhoid-like illness with bloody diarrhea and possible fever, nausea, comiting, colonic ulcerations and terminal ileum nodularity.
  2. Septicemia (rarely)

Has been mistaken for salmonellosis and inflammatory bowel disease

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70
Q

Species and habitat for Salmonella

A

Lower animals (Poultry, cows, pigs, pets) for non-typhoid strains. Humans for ​S. Typhi​.

​

All serotypes are considered a single species

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71
Q

The (5) characteristics of Salmonella

(lactose fermenter or non-fermenter? How does it plate on TSI? How is it transmitted?)

A
  1. Non-lactose fermenter
  2. Produces hydrogrn sulfide (black)
  3. Transmission via improper food handling (usually poultry/poultry products; reptiles as well)
  4. Found in humans and livestock
  5. Secondary transmission person-to-person
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72
Q

The (5) Clinical Syndromes of Salmonella

A
  1. Asymptomatic (carrier) state
  2. Febrile Gastroenteritis (**Most common presentation**)
  3. Enteric Fever
  4. Septicemia
  5. Focal Infections (osteomyelitis, endocarditis, etc.)
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73
Q

What types of Salmonella cause enteric fever?

A

S. Typhi and S. paratyphi

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74
Q

What patients are most at risk for septicemia from Salmonella? (5 pt. types)

A

Patients with underlying:

  • Leukemia/ lymphoma
  • AIDS
  • Lupus (SLE)
  • sickle cell crisis
  • alcoholic hepatitis
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75
Q

Key dermalogical sign of enteric fever

A

Rose spots (pink macules or prupuric lesions)

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76
Q

Clinical syndromes associated with Citrobacter (3)

A

Nosocomial infections of (1) urinary and (2) respiratory tracts of debilitated, hospitalized patients. Can also cause (3) endocarditis.

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77
Q

​What are C. freundii ​and C. koseri, ​and what can they each cause?​

A

Species of Citrobacter

C. freundii: rare cause of diarrhea

C.koseri: rare cause of meningitis and brain abscess in neonates

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78
Q

What are the 10 types of enterobacteriaceae?

A
  1. E. Coli
  2. Shigella
  3. Salmonella
  4. Edwardsiella
  5. Citrobacter
  6. Klebsiella
  7. Enterobacter
  8. Serratia
  9. Proteus
  10. Yersinia
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79
Q

What are the (3) Genuses under Klebsielleae?

A
  1. Klebsiella
  2. Enterobacter
  3. Serratia
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80
Q

Nosocomial diseases

A

Diseases originating in the hospital

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81
Q

The (4) Klebsiella types and their associated clinical syndromes:

A
  • ​(1.) ​K. pneumoniae and (2.) K. oxytoca: Primary lobar pneumonia​ characterized by destructive changes to lungs (necrosis, hemorage [jelly sputum], etc.) as well as UTI’s
  • (3.) K. ozaenae​- atrophic rhinitis + destruction of mucosa
  • (4.) K. rhinoscleromatis​- rhinoscleroma, chronic granulomatous disease involving upper respitaroy tract
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82
Q

Clinical syndromes associated with enterobacter

A

Frequent colonizers of hospital patients, casuing opportunistic infections involving urinary tract, respiratory tract, and cutaneous wounds (occasional septicimeia and meningitis)

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83
Q

Most important species of and clinical syndromes associated with Serratia ( 2 main groups of effects)

What color does it plate?

A

S. marcescens

(Produce red colonies)

​General Effects of enterobacteria: Nosocomial infections, pneumoniae, epticemia, etc.

Also can cause endocarditis and osteomyelitis in IV drug addicts

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84
Q

The 2 most important species of Proteeae and the (2) ID features associated with them both.

A

P. mirabilis and P. vulgaris

(1) Swarming observed on blood agar (due to growth in spurts) and (2) strongly urease positive

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85
Q

Proteus Clinical Syndromes (Syndromes for P. mirabilis? Syndromes for P. vulgaris)

A

P. mirabilis: most frequently isolated (second only to E. Coli). Cause of UTI and wound infections. Alkaline urea (due to urease) can lead to renal calculi (kidney stones from struvite– staghorns).

P. vulgaris​: most commonly recovered from infected sites in IC patients

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86
Q

Key Lab ID feature of Yersinia enterocolitica

What is the main reservoir associated with Y. enterocolotica

A

Pinpoint colonies on MacConkey at 24 h

Pigs are a major reservoir for human infection (chitterlings).

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87
Q

Clinical syndromes associated with Yersinia enterocolitica

A

Associated with diarrheal disease and acute enterocolitis. Can mimic appendicitis.

Also associated with transfusion related sepsis and infections, as it can proliferate in blood stored at 4 degrees C, after 2-3 weeks.

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88
Q

Name the five genera of Enterobacteriaceae that can cause gastrointestinal disease.

A
  1. E. coli
  2. E. tarda (Edwardsiella)
  3. Citrobacter (C. freundii)
  4. Salmonella/Shigella
  5. Y. enterocolitica
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89
Q

(7) Key structural/cultural characteristics used by both Neisseria forms

A
  1. Gram-negative
  2. Kidney bean diplococci
  3. LPS
  4. Pili
  5. Required enriched media (VPN or Chocolate agar)
  6. Oxidase positive
  7. Glucose consumption
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90
Q

What is the difference in sugar oxidation between N. gonorrhoeae and N. meningitidis?

A

Although they both oxidize glucose only menigitidis oxidzies maltose.

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91
Q

6,000- fold increaase risk for meningococcal and disseminated gonococcal disease in persons with deficiency of…

A

One or more of the terminal components of ​Complement (C5-9)

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92
Q

Key virulent components of Neisseria meningitidis:

A
  1. Polysaccharide capsule
  2. LOS (N. meningitidis version of LPS): responsible for cell damage and systemic inflammation
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93
Q

Main (2) clinical manifestations of Neisseria meningitidis infection + presentation for each

What is another key manifestation?

A
  1. Meningococcemia (shock; hemorrhage; purpura; adrenal hemorrhage)
  2. Meningitis (headache; AMS; neurological signs; skin petecheae/purpura)

Urethritis

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94
Q

What culture results make you lean towards Neisseria meningitidis as a diagnosis?

A
  1. Oxidase positive
  2. Oxidation of glucose
  3. Oxidation of maltose
  4. Growth on nonselective media (blood or chocolate agar)
  5. Growth enhanced in CO2
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95
Q

Neisseria meningitisis treatment (2)

A

Penicillin (resistance is uncommon); ceftriaxone can also be used and it cross BBB

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96
Q

What drugs are used for chemoprophylaxis for household contacts of individuals diagnosed with Meningitis? (3)

A
  1. Rifampin
  2. Ciprofloxacin
  3. Ceftriaxone (1 dose)
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97
Q

The 4 key antigenic structures of Neisseria gonorrhoeae + their location

A
  1. Pili (adhesion)
  2. PorB (Pores which facilitate epithelial cell invasion)
  3. Opa (adherence proteins)
  4. Rmp proteins (stimulate blocking antibodies)

All located in the outer membrane

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98
Q

Gonorrhea is a [intracellular/ extracellular] pathogen

A

INTRACELLULAR.

Tends to invade PMNs

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99
Q

Location where N. Gonorhea use Pili? Opa proteins?

A

Pili: urethral and vaginal epithelium, nonciliated fallopian tube epithelium, sperm, neutrophils

Ops proteins​: cervical and urethral epithelium and other gonoccocal cells

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100
Q

Most common sign of localized gonorrhea for men (in general)? For women? For gay men?

A

Men: Urethritis

Women: Cervicitis

Gay Men: Prostatitis

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101
Q

Most common manifestations of disseminated gonorrhea

A

Pelvic Inflammatory Disease (women); Arthritis

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102
Q

What is the main clinical specimen used for direct detection for gonorrhea clinical specimens?

A

Nucleic acid amplification of a ​urine specimen

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103
Q

What drugs are used for treatment of Gonorrhea?

A

Ceftriaxone- single dose (NO ORAL TREATMENT!)

PLUS​ azrithromycin (single dose) or Doxycycline (7 days) for co-infection with Chlamydia

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104
Q

N. Gonorrhea and Penicillin

A

Usually Gonorrhea is penicillin resistant due to PBP and B-lactamase (PPNG) alterations

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105
Q

What gram type is haemophilus? Where is it found? Capsule or no Capsule?

A

Encapsulated gram-negative coccobacilli found in the respiratory tract.

106
Q

Main capsule type for Haemophilus influenzae

A

Type B

107
Q

Haemophilus influenzae type b: Clinical Manifestations (4)

Nontypable H.I. manifestations (3)

A
  1. Meningitis
  2. Epiglottis (cherry red epiglottis)
  3. Cellulitis
  4. Arthritis

(usually in young children around 2-4)

Non-typable:

Otittis media

Sinusitis

Bronchitis

108
Q

Lab Diagnosis of Haemophilus influenzae

(Gram stain of what? Cultrue type? Motility? Spore-formation? Growth factors?)

A
  • Gram stain- CSF, joint fluid
  • Culture- chocolate agar
  • Nonmotile, non-sporeforming
  • ​Require growth factors from lysed blood​
    • X factor (hematin) “hema-TEN”
    • V factor (NAD) “N = nickle”
109
Q

25-50% of Haemophilus influenzae is resistant to _______ because of the production of _______.

A

Ampicillin

Beta-lactamase

110
Q

Haemophilus influenza vaccine is often conjugated to what things? (3)

A
  1. Diphtheria toxoid
  2. N. memingitides OMP
  3. Tetanus toxoid
111
Q

Bordetella pertusis is aka…

A

Whooping cough

112
Q

Is Bordetella pertusis Gram + or - ?

A

Negative

113
Q

What are the 4 main toxins associated with Bordetella pertusis?

A
  • Pertussis toxin (PT)
  • Tracheal cytotoxin (peptidoglycan fragment)
  • Dermonecrotic toxin (causes ischemic necrosis)
  • Endotoxin (LPS)
114
Q

What are the 2 main adhesin types associated with Bordetella pertusis?

A

Pertactin and Filamentous hemagglutinin (Fha)

115
Q

Mechanism of action (2) of Pertussis Toxin and clinical manifestations

A

Made from AB subunit

  • “A” catalyzes ADP ribosylation of a G-protein, preventing inactivation of adenylate cyclase, leading ​increased respiratory secretions, mucus production and lymphocytosis
  • “B” binds to receptors on ciliated respiratory cells and phagocytic cells
116
Q

Adenylate Cyclase Toxin

A

Affliated with Bordetlla Pertussis

Causes increase cAMP levels in cells affecting leukocyte function

117
Q

Who often acts as the reservoir for Bordella pertussis?

A

Adults because they don’t classic symptoms

118
Q

The 4 stages of Bordella Pertussis and what occurs at each stage

A
  1. Incubation
  2. Catarrhal (Rhinorrhea, malaise, fever, sneezing, anorexia)
  3. Paroxysmal (coughs w/ whops, vomiting, leukocytosis)
  4. Convolescent (diminished cough, development of secondary complications)
119
Q

Main method used for B. Pertussis ID in lab

A

PCR

120
Q

What is used in treatment of Bordetella pertussis? What effect does this have on the disease state/ epidemiology?

A

Azithromycin is effective in early disease.

It eliminates nasopharyngeal organisms and prevents spread but it ​does not alleviate the cough.

121
Q

What vaccines are recommended for Bordetella pertussis (2)?

A
  1. DTaP for all children
  2. Tdap for all adults
122
Q

Pseudomonas aeruginosa habitat

A
  • Environmental organism
  • Grows in moist, unsterile areas (cut flowers, hot tubs, toilets, mops etc.)
123
Q

Describe the type of patients who acquire Pseudomonas aeruginosa infections (4)

A
  1. Burn Patients
  2. Cystic fibrosis patients
  3. Patients with hematologic malignancies
  4. Immunocompromised patients
124
Q

List the major toxins produced by Pseudomonas aeruginosa and describe their principle effect on human cells (3)

A
  1. Exotoxin A: Blocks protein synthesis, contributing to dermatonecrosis in wounds and tissue damage in lungs
  2. Exoenzyme S: ADP-ribosylating toxin. Epithelial cell damage facilitates bacterial spread, tissue invasion and necrosis
  3. Elastase: ​Results in tissue destruction and hemorrhagic lesions (ecthyma gangrenosum). Las A nd Las B enzyymes act synergistically to degrade elastin . Degrades compliment components and inhibits neutrophil chemotaxis and function.
125
Q

List the diseases associated with Pseudomonas aeruginosa (9)

A
  1. Folliculitis (hair follicle infection)
  2. Nail Infections
  3. Severe necrotizing bronchopneumonia
  4. UTIs
  5. Ear infections (swimmers ear)
  6. Eye infections
  7. Bacteremia (Ecthyma gangrenosum)
  8. Endocarditis (IV Drug Users)
  9. Osteomyelitis
126
Q

Ecythyma gangrenosum

A

–EG is a well-recognized but uncommon cutaneous infection most often associated with a Pseudomonas aeruginosa bacteremia.

–EG usually occurs in patients who are critically ill and immunocompromised and is almost always a sign of pseudomonal sepsis.

127
Q

Diagnosis of P. aeruginosa (culture type/appearance; ID characteristics)

A
  • Grows on blood and MacConkey agar producing colonies with metallic sheen
  • Green colored
  • Grape-like odor
  • Oxidase positive
  • Grows at 42 degrees C
128
Q

Name the non-fermenters that are named on the biothreat agent list

A
  1. Burkholderia pseudomallei
129
Q

Burkholderia pseudomallei Melioidosis can present itself in what 3 ways?

A
  1. Acute disease (septicemia + metastatic lesions) 95% mortality
  2. Subacute disease (most common). TB like pneumonia with cellulitis and lymphangitis
  3. Chronic Disease: Localized chronic cellulitis. Treated with antibiotics prior to draining otherwise becomes bacteremic.
130
Q

Discuss the association of Burkholderia cepacia and pulmonary infection in cystic fibrosis patients

A

Mutation in CFTR results in defects in innate immunity, increased airway inflammation and sticky mucus which provides an ideal niche for chronic lung infection. Chronic lung infection accounts for 85% of deaths with CF and B. cepacia is one of the top pathogens that lead to infection (along with S. aureus and P. aeruginosa)

131
Q

What is pulmonary exacerbation?

A

Cellular defect from CF results in increased mucus thickness and thus impaired innate immunity within lungs. This leads to exacerbation by recruitment o neutrophils, cytokines and neutrophil elastases which cause signficant lung pathology.

132
Q

Burkholderia cepacia is affliated with what disease types?

A

Respiratory tract infections (major issue for patients with CF); UTIs; Septicemia

133
Q

Main disease associated with Burkholderia pseudomallei

A

Melioidosis

134
Q

Diseases associated with Stenotrophomonas maltophilia

Where is S. maltophilia usually aquired?

A
  • Opportunistic infections (bacteremia, UTI’s, etc.)
  • Usually respiratory infections

Usually hospital acquired and causes systemic infections in debilitated patients because it is very resistant to antibacterials

135
Q

What is unique about the growth of S. maltophilia?

A

It is a non-fermenter that is oxidase negative.

136
Q

Diseases associated with Elizabethkingia meningoseptica?

Location?

Resistance?

A
  1. Associated with neonatal meningitis
  2. Pneumonia in adult (usually IC) patients

Usually nosocomial. Outbreaks traced to breast pumps used in hospital nurseries

Very Resistant

137
Q

Diseases associated with Acinetobacter baumannii

A

Implicated in community acquired and nosocomial infections

138
Q

Key identifying characteristics of Bacillus (4)

Is it motile? Any exceptions?

A
  1. Spore forming Gram positive rod
  2. Widespread in nature
  3. Prefers aerobic conditions
  4. Motile except for B. anthracis
139
Q

Epidemiology of Bacillus anthracis (biothreat category, spread)

A
  • Category A biothreat agent
  • Spreads via:
    • Inoculation (95%): contaminated soil or infected animal products
    • ​Inhalation: Wool sorters disease; processing goat hair; biological weapons
    • Ingestion
      *
140
Q

Clinical presentation of Bacillus anthracis

A
  1. Necrotic eschar
  2. GI anthrax: Upper GI: ulcers in mouth/esophagus; Lower GI: N/V malaise, bloody diarrhea
  3. Inhalation Anthrax: Initial symptoms are nonspecific (flu-like); second stage symptoms include edema and enlargment of mediastinal lymph nodes (accounting for widened mediastinum observed on chest X-ray)
141
Q

Key toxins of Anthrax

A

Edema Toxin and Lethal Toxin

142
Q

The 3 distinguishing biochemical markers of anthrax

A
  1. Motility negative
  2. Non-hemolytic
  3. PCN susceptible
143
Q

The 3 forms of anthrax disease

A
  1. Inhalation
  2. GI
  3. Cutaneous
144
Q

Name the 2 aerobic Gram-positive rods that can cause food poisoning

A
  1. Bacillus cereus
  2. Listeria
145
Q

Describe the key ID characteristics of Listeria monocytogenes (7*)

(*3 of them are motlity related)

(spore-forming? Gram-staining? Where does it live? Catalase? Motility?)

A
  1. Non-spore forming
  2. Gram-positive rod
  3. Can live in animals and refrigerated foods
  4. Catalase +
  5. Tumbling motility
  6. Umbrella motility
  7. Motile at root temp
146
Q

ActA gene and Listeria

A

ActA gene is utilized to move bacteria into adjacent cells without exposure to immune system by using the actin of cells

147
Q

Explain why patients with defects in cellular immunity are particularly susceptible to infections with Listeria monocytogenes and list three patient populations that are at risk for listeriosis (+ what happens to them?)

A

Listeria moves from cell to cell so is rarely ever exposed enough for antibodies (humoral response) to have a major effect.

Neonates (early granulomas, late menigitis) Elderly (flu-like + or - gastroenteritis) and Pregnant women/ patients with cell-mediated immune defects (bacteremia or disseminated disease with hypotension/meningitis) are most at risk.

148
Q

Key identifying characteristics of Erysipelothrix rhusiopathiae (5)

(what does it look like? aerobic or anaerobic? Growth speed? hemolysins? Production on TSI?)

A
  1. Pleomorpic gram postive rods that form long filaments (“hairlike”)
  2. Facultative anaerobe
  3. Slow growth (2-3 days incubation)
  4. Small, grayish, alpha-hemolytic ​colonies
  5. Produces H2S on triple sugar iron (TSI) agar
149
Q

Epidemiology of E. rhusiopathiae

A
  1. Ubiquitous in soil and groundwater
  2. Widely recognized in animals but human disease is uncommon
  3. Human infection is aquired from occupational working with animals (butcher, vet, etc.)
150
Q

Diseases associated with E. rhusiopathiae (2)

A

Cutaneous infections after subcutaneous inoculation

Two forms:

  1. Erysipeloid​: localized skin infection on fingers/ hands. Slowly spreads peripherally
  2. Septicemic​: uncommon; frequently associated with endocarditis
151
Q

Characterisitcs of Corynebacterium

A
  1. gram positive rods
  2. clumps of organisms resembling chinese letters
  3. Commonly called “diphtheroids”
152
Q

Epidemiology of Corynebacterium? (location, spread, etc.). What are the important species?

A

​Location​: Colonize skin, upper respiratory tract, GI tract, GU tract

Spread​: infection transmitted by respiratory droplets or direct contact with cutaneous infection (rare in US due to vaccine)

Important Species​: C. diphtheriae; C. jeikeium

153
Q

Clinical manifestation of Corynebacterium diseases (what do the toxins inhibit? where can they circulate? what does it lead to?)

A

Disease caused by potent exotoxin which inhibits protein synthesis.

Leads to pharyngitis with patchy exudates on tonsils, uvula and soft palate (leathery skin). Toxins can circulate to the CNS or heart causing injury.

154
Q

C. jeikeium and resistance

A

A species of Corynebacterium.

Infects immunocompromised patients. Resistant to most antibiotics (except vancomycin)

155
Q

Characteristics + key clinical manifestion of Arcanobacterium hemolyticum (what does it cause? Who is it isolated from?)

A
  • Beta-hemolytic (similar to group A Strep)
  • Isolated mostly from young adults
  • curved, club-shaped or “V” formation Gram-positive rod

Appears very similar to group A strep

Causes fever, rash, pharyngitis. Isolated from wounds/ blood of patients with septicemia and endoarditis.

156
Q

Main difference between Listeria and Strep

A

Listeria is catalase +

157
Q

Key characteristics of Nocardia species (gram-positive or negative? Aerobic or anaerobic? Incubation? Cell wall? Best stain for it?) (5)

A
  1. Gram-positive
  2. Cell wall with mycolic acid
  3. Strict aerobe
  4. Prolonged incubation
  5. Partial acid-fast

Type of actinomycete

158
Q

Epidemiology of Nocardia? Who is the disease most common in?

A

Worldwide distribution in soil. Infection via inhalation or traumatic introduction.

Disease most common in pts with chronic pulmonary disease or immunocompromised pts. with T-cell deficiencies

159
Q

Diseases associated with Nocardia (3)

A
  1. Pulmonary disease
  2. Primary or secondary cutaneous infections
  3. Secondary CNS infections
160
Q

Diseases associated with Rhodococcus

A
  1. Pulmonary diseases
  2. Opportunistic infection (wounds, peritonitis, etc.)
161
Q

Disease associated with Tropheryma

A

Whipple’s Disease

162
Q

Pathogenicity of Treponema pallidum

Visble in light Microscopy?

Vector/ Reservoir?

Transmission?

Disease?

A

Visble in light Microscopy: No (darkfield is best)

Vector/ Reservoir: None

Transmission: Intimate sex/ contact

Disease: Syphilis

163
Q

Pathogenicity of Leptospira interrogans

Visble in light Microscopy?

Vector/ Reservoir?

Transmission?

Disease?

A

Visble in light Microscopy: ​No (darkfield is best)

Vector/ Reservoir: ​​Rodents, dogs, swine, cattle

Transmission: ​Contact or ingestion of urine-contaminated water

Disease: Leptospirosis

164
Q

Pathogenicity of Borreli recurrentis

Visble in light Microscopy?

Vector/ Reservoir?

Transmission?

Disease?

A

Visble in light Microscopy: ​Yes

Vector/ Reservoir: ​Lice, ticks, rodents

Transmission: ​Ticks or lice

Disease: ​Relapsing fever

165
Q

Pathogenicity of Borrelia burgdorferi

Visble in light Microscopy?

Vector/ Reservoir?

Transmission?

Disease?

A

Visble in light Microscopy: ​Yes

Vector/ Reservoir: ​​Ticks, mice, deer

Transmission: ​​Ticks

Disease: Lyme disease (lyme borreliosis)

166
Q

Describe the pathogenesis of Syphilis infection (how does it enter the body? when symptoms begin? describe the pathogenic lesion?)

A
  • passes through intact mucosa or abraded skin
  • symptoms occur when number of organisms reach critical mass (10-90 days post inoculation)
  • pathogenic lesion is obliterative endarteritis (leading to blockage of arterial vessels)
167
Q

Describe the presentation of primary syphilis

A

An ulcerative lesion at site of inoculation (chancre) with regional adenopathy (node enlargment). Heals spontaneously.

168
Q

Describe the presentation of secondary syphilis

A

Systemic flu-like illness which may develop 2-10 weeks after primary lesion heals. Fever, papulosquamous rash and generalized lymphadenopathy along with spread to almost all local sites.

169
Q

How does congenital syphilis present at birth? Later in life?

A

The child is actually normal at birth​.

Multisystem diseases occur later in life inlcuding rhinitis (nasal snuffling), rashes, issues with bone and cartilage involvement (teeth) and CNS, liver and spleen issues.

170
Q

The two types of tests which lead to a diagnosis of Syphilis

A

Nontreponemal Tests: Not specific to just syphilis. Screens for antibodies against cardiolipin (which is part of T. palidum) “Venereal Disease Research Laboratories (VDRL)” or “RPR”

​Specific Treponemal Serology Tests​: Measure specific antibody against T. pallidum (ex. Fluorescent Treponemal Antibody- Absorption Test (FTA-Abs or TPPA (MHA-TP))

171
Q

Treatment of Syphilis

A

It’s extremely sensitive to penicillin

172
Q

Jarisch-Herxheimer Reaction

A

Caused during death of T. pallidum

Release of toxic products from killed spirochetes. Causing fever, chills, headache and hypotension.

173
Q

What is the mechanism for relapsing fever?

A

B. recurrentis and related organisms escape immune recognition by altering their antigenic structure during infection (S and E segments)

Resolves in 3-5 days, remits after 7-9 days. Each relapse is less severe.

174
Q

What are the (2) primary reservoirs for lyme boreliosis (borrelia bergdorferi)? What spreads it?

A

Deer and white footed mouse –> reservoirs

Spread by tick

175
Q

Clinical manifestation of Lyme Disease (early, early disseminated, late)

A

Early​: erythema migrans (bulls-eye rash); flu-like symptoms

​Early Disseminated​: fatigue, headache, fever, malaise, neuropathies (facial nerve paralysis)​, heartblock

​Late: Arthritis; Encephalopathy (memory loss, cognitive defects, etc.)

176
Q

How is Leptospirosis acquired?

A

A zoonosis affecting a variety of animal species. Humans acquire the organism by contact with infected animal urine, usually through contaminated water (often water sports)

177
Q

Leptospirosis pathogenesis

A

After infection, spirochetes invade bloodstream and affect endothelial cell integirty causing vasculitis in many organs. Immune complexes found in kidney.

178
Q

Clinical Manifestations of Leptospirosis (3 stages)

A

First Stage​ (bacteremia- bug in blood): fever, headache, conjunctival suffusion

​Second stage ​( immune- bug no longer in blood/CSF, only urine): aseptic memningitis or generalized illness with headache, rash, etc.

​Severe​: (stages blend) Prominent hepatitis, kidney involvment, hemorrhage

179
Q

How does Treponema pallidum move?

A

Axial fibril (internal flagellum)

180
Q

Syphilis and self-limitation

A

Primary and secondary stages of lymphocytes are self-limiting

181
Q

Natural History of Untreated Syphillus

A

1/3rd of pts resolve the infection

1/3 convert to latent

1/3rd go to tertiary syphilis (neuro, cardiovascular, gummatous)

182
Q

List the animal vectors associated with:

Brucellosis

Plague

Tularemia

Pasteurellosis

A

Brucellosis​: Goats, sheep, camels, pigs, cattle, dogs

Plague​​: Fleas, rodents/small animals

Tularemia: Voles, Lagomorphs (rabbits), ticks, deer flies, mosquitoes​

Pasteurellosis​: All types of animals but especially ​cats and dogs

183
Q

Human populations at risk for Brucellosis

What level of Bioterrorism Agent is it?

A
  1. Those who consume unpasteurized dairy products
  2. Contact with infected animals (slaughterhouse workers, vets, farmers)
  3. Lab workers

Category B Bioterrorism Agent

184
Q

Describe the disease conditions associated with infections caused by Brucella (basic pathogenesis, clinical manifestations (initial + advanced)

A

Pathogenesis​: Organisms are phagocytized by macrophages and carried to spleen, liver, etc. Host forms small granulomas and pathogen survives within cell.

Clinical Manifestations​: Initial is non-specific (flu-like); Unudulant fever (fever of unknown origin [FUO]); splenomegaly, hepatomegaly, etc.; Advanced: GI issues, Osteolytic lesions, respiratory symptoms.

185
Q

Key culture characterisitics of Brucella (size, shape, gram status, growth speed, media)

A
  • Small coccobacillary Gram negative rod.
  • Slow growing
  • Requires enriched media (chocolate agar) to grow and prolonged incubation
186
Q

Describe the populations at risk for Zoonoses caused by Francisella tularensis and identify within the USA where tularemia is endemic.

Is there a vaccine available?

A

Hunters, lab workers, people exposed to ticks. Most patients are men (because men hunt more often)

Parts of US where endemic: Arkansas, Ohlahoma, and Missouri

Vaccine? Yes

187
Q

Describe the disease state associated with Tularemia (pathogenesis + clinical manifestations( 5))

Where is this on the biothreat list?

A

Pathogenesis: Organsims enter through breaks in the skin and an ulcer​ may develop at the entry site. Organisms disseminate via bloodstream and host response is granuloma formation. Facultative intracellular organism.

Clinical Manifestations​: Usually ulceroglandular (papule at site that is necrotic and ulcerates). Could be oculoglangular, typhoidal​, pneumonic infection, ​glandular (adenopathy)​, oropharyngeal –> all depends on method of exposure

Category A biothreat

188
Q

Culture characterisitcs of Francisella tularensis. (size, shape and gram status? aerobic vs anaerobic? media? Color? Incubation period? )

A
  • Very small gram-negative coccobacilli
  • Cannot be isolated on routine media (​requires cystein supplemented media​). Can also be recovered on chocolate agar and charcoal yeast extract (CYE)
  • Strict aerobe
  • Pearly white colonies with slight greening of agar below
  • Long incubation (up to 3 weeks)
189
Q

Describe the disease state associated with pasteurella (how its spread and clinical manifestations)

A

Spread: ​Associated with cat and dog bites/scratches. May be aquired by respiratory route.

​Clinical Manifestations​: Painful swelling, redness, cellulitis. If the wound is very deep ​septic arthritis, osteomyelitis or even fasciitis (in compromised hosts) can occur.

190
Q

Culture characteristics of Pasteurella multocida (size, shape, aerobicity, media, odor, oxidase status, catalase status)

A

Small bipolar Gram negative rods

Facultative anaerobe

Grows on blood and chocolate but not​ MacConkey

Large “buttery” colonies w/ moth ball odor

Most species are ​oxidase-positive​ and catalase-positive

191
Q

Epidemiology of the plague (The 2 endemic forms and how it spreads)

What category bioterrorism agent is it?

A

Two endemic forms: **​Urban Plague_​**​_​- maintainted in rat pop.. Spread to humans by fleas. ​Sylvatic Plague-endemic ( western USA)​. Carried by prairie dogs, mice, rabbits and rats.

Often times spread to human by domestic cats or otherwise fleas

Category A bioterrorism agent

192
Q

Disease state of Plague (pathogenesis + clinical manifestations for each plague type (3) )

A

​Pathogenesis: ​Facultative intracellular organisms; causes enlarged tender lymph nodes with hemorrhagic necrosis (black buboes); terminal cyanosis​ (Black death)

​Clinical Syndromes: ​

  1. Bubonic Plague​: Fever + painful bubo days after bite; fever chills, weakness and intense pain
  2. Septicemic Plague​: Direct infection of bloodstream; fever, delirium, seizures, septic shock; Black hemorrhagic splotches (Black death)
  3. Pneumonic Plague​: plague bacillus reaches lung. Respiratory signs of infection (cough, chest pain, hemoptysis, infectious sputum)
193
Q

Culture characteristics of Yersinia pestis​ (plague) (oxidase, size and shape, speed of growth)

A

oxidase negative; cells look like safety pins (small, cocco-bacillary); small pinpoint coloneysin 24 hours ( but fried egg under microscope if left out); slow growing on ordinary media

194
Q

Is there a vaccine for Yersinia pestis?

A

Yes; only for high risk patients

195
Q

Unusually fact about Pasteurella treatment

A

It is very susceptible to penicillin, which is unusually because it is gram-negative (which tends to put up a bigger fight to penicillin due to the outer wall)

196
Q

Staining for rickettsii

A

Giemsa

197
Q

Why is rickettsia an obligate intracellular?

A

It requires host NADP+, COA, and ultimately ATP in order to function

198
Q

Why is coxiella not killed when a phagosome containing it fuses with an endosome?

A

Coxiella actually requires a slightly lower pH, so fusion with a phagosome promotes its function

199
Q

Which rickettsia does not migrate using actin polymerization?

A

R. Prowazekii

200
Q

What causes the red rashes affliated with the ricketsia’s?

A

Bacteria multiply in endothelial cells lining small blood vessels. Rupture results in rash and primary lesion (vasculitis)

201
Q

Cause and clinical manifestation of Rocky Mountain Spotted Fever

A

Rickettsia rickettsii (intracellular; replicates in cytoplasm and spreads via actin polymerization)

Syndromes​: Rash on extremities, high fever, headaches

202
Q

Epidiemiology of Rocky Mountain Syndrome (vector, time of transmissionwhen is it most common, where is it most common)

A

​Vector: Hard ticks​ (dog, wood) are vectors; transmission requires prolonged contact.

When​: most common in summer

Where: Southeast atlantic, south central states

203
Q

What is the cause for Rickettsialpox? What are the clinical manifestations? Describe the two phases.

How is it resolved?

A

Rickettsia akari

Clinical Manifestations​: Mild disease with vesicular rash; self limiting

2 phases: phase 1: firm red papule at site of bite which develops into vesicle then black eschar as bacteria spread​​. phase 2: high fever, headache, myalgias, photophobia etc.​

Self-limiting after 1 week; no deaths reported

204
Q

Epidemiology of Rickettsialpox (vector, where is it found?)

A

Vector is bloodsucking mites, found on mice

Found in northern USA, Russia, Africa, Korea

205
Q

Cause of Epidemic typhus? Clinical manifestations?

A

Rickettsia prowazekii

​Manifestations​: Fever, headache, myalgias; maculopapular rash (first on the trunk then spreads to extremities)

206
Q

Epidemiology for Rickettsia prowazekii (location, spread, reservoir, vector)

A
  • Present in central and south america, and africa
  • Disease associated with unsanitary conditions (peaks in winter)
  • ​Tranmission by body louse (vector)
  • Reservoir –> humans + flying squirrels
207
Q

Brill-Zinsser

A

Relapse of epidemic typhus. Can appear 10-40 years later

208
Q

Cause of Murine Typhus (Endemic Typhus)

What are its clinical manifestations?

A

R. Typhi

Manifestations​: Abrupt fever, severe headache, chills, myalgia. Late rash in 50% of cases

209
Q

Endemic Typhus Epidemiology (vectors, reservoirs, where is it found?

A

Vectors: ​Rat flea; cat flea ​

​Reservoirs​: Rodents

Found in temperate and subtropical coastal areas

210
Q

Cause of Scrub Typhus.

Clinical Manifestations

A

Orientia tsutsugamushi

Manifestations​: Maculopapular rash after 5 days, lymphadenopathy; fever; headache. Necrotic eschar 50-80% of the time.

211
Q

Epidemiology of Scrub Typhus (location, vector/reservoir, spread)

A

(caused by orientia tsutsugamushi)

Found in the Far East (southwest pacific, southeast asia, japan)

Mites are the vectors and reservoir

Passaged to progeny via infected ova

212
Q

What are the 2 types of Ehrlichiosis? What is different between them?

A

Human anaplasmosis (HA) and Human monocyte ehrlichiosis (HME)

HA:​ granulocytes primarily infected (Neutrophils, eosinophils, basophils)​

HME​: monocytes, mononuclear phagocytes

213
Q

Pathology and clinical manifestation (7) of Ehrlichiosis

Name the 2 bodies. What does this smaller body assemble?

A

Pathology​: Infect circulating leukocytes; 2 polymorphic forms (smaller elementary bodies and larger reticulate bodies)

Elementary bodies assemble morulae

Manifestations​: Flu-like illness; high fever; headache; typically no rash; leukopenia; thrombocytopenia; elevated serum transaminases (sometimes late onset)

214
Q

Cause and Clinical manifestation of Q-fever

A

Coxiella burnetii

  • Clinical features​: Most human infections are NOT apparent. ​No rash​. Mild, dry cough and pneumonia; abrupt onset of fever, chills, headache at 9-20 days.
  • Resistant to drying; growth at low pH
  • Fatalities are rare; subacute endocarditis is rare
215
Q

Epidemiology of Q-fever (transmission, carriers, geographic distribution)

A

Transmission from animals to humans by inhalation of (fecal) dust.

Carried by large mammals (cattle, sheep, goats, etc.)

World-wide distribution

216
Q

The key spore forming Gram Positive Anaerobes (4 ) hint: all are related

A
  1. Clostridum perfringens
  2. Clostridium tetani
  3. Clostridium botulinum
  4. Clostridium difficle
217
Q

What are the 3 disease that are affliated with Clostridium perfringens?

A
  1. Gas gangrene (classically affliated)
  2. Intraabdominal infections
  3. Food poisoning
218
Q

Strucure of C. perfringens (gram status, motility, encaspulation, spore status, hemolytic status, shape)

A

–Gram positive, “box car” shaped
–Non-motile
–Encapsulated
–Forms spores
–Double zone hemolysis

219
Q

Gas Gangrene (pathogenesis, clinical presentation, treatment)

A

Pathogenesis​: Trauma with devitalized tissue/muscle; spores from C. perfringens (and other bacteria) enter, germinate and quickly release toxins (alpha and iota)

Clinical manifestation​: rapid onset; necrosis; bullae formation; crepitis (skin pops upon palpation)

Treatment: ​DEBRIDEMENT​

220
Q

Main type of C. perfringens involved in Gas gangrene and its main associated toxins (2)

A

Type A is the most common cause

​Alpha and Iota Toxins​ are the most key

Alpha​- lysis of inflammatory cells (white cells) and tissue destruction

Iota​- necrosis and vascular permeability

221
Q

Clostridium tetani pathogenesis + clinical manifestation

A

Spores enters via puncture wounds, burns, umbilicus etc. which bring it to an anaerobic environment.

There is local germination without necrosis

​The tetanospasmin neurotoxin is the thing which has pathogenic effects

​​Clinical Manifestation​: lock jaw, opsithotonus (classic full body flexion).

222
Q

Treatment/ Prevention of Tetanus

A

Human tetanus immunoglobulin (HTIG) –> binds up free toxin

Vaccine is available as well (every 10)

223
Q

One of the most common ways that C. botulinum is delivered

A

Home canning of foods because the spores are extremely heat resistant so if you don’t apply pressure + heat for a long time, preformed toxins may contaminate the food.

224
Q

What is the most potent toxin in nature?

How does it work?

A

Clostridium botulinum

Blocks acetylcholine release by cleaving snares

225
Q

What is distinct about the clinical presentation of Botulism?

What is the treatment for Botulism?

A

Descending paralysis, flaccid in nature

(cranial down)

Antitoxin + supportive treatment

226
Q

The two key toxins of C. Dif

A

Toxin A (enterotoxin, inflammatory response, major toxin)

Toxin B (cytotoxic)

227
Q

Clinical presentation of C. dif (6)

What is the dominate strain of C. dif in the US?

A
  1. Pseudomembranous colitis
  2. Diarrhea (watery/bloody)
  3. Abdominal pain
  4. ​Leukocytosis
  5. Fever
  6. Toxic megacolon (may require colectomy)

BI (Nap1) Strain = dominate in U.S.

228
Q

Standard for C. dif detection

What is the treatment?

A

PCR (amplifies toxin region)

Very sensitive and specific

Treated with ​Vancomycin; sometimes colon resection or fecal transplant is needed; stop other antibiotics if possible​

229
Q

What is the main gram negative anaerobe?

A

Bacteroide fragilis

230
Q

Necrosis and Clostridium tetani

A

You have local germination without necrosis in C. tetani

231
Q

Key clinical manifestations of B. fragilis

What types of infections are they commonly associated with?

A

Hallmark is abscess formation​

This is almost always a mixed infection, filled with pus of PMN’s, fibrin, and debris/necrotic tissue.

Most ofen associated with intraabdominal infection and in wound infection (skin and soft tissue)

232
Q

What are the 2 most important aerobes and anaerobes we encounter clinically?

A

E.coli (aerobe) and B. fragilis (anaerobe)

233
Q

(5) key differences between Bacteroides and Prevotella:

A

These are very similar and both only cause harm if they end up in the wrong place. Except unlike bacterioides, ​Prevotella​…

  1. has no virulence factors
  2. normally lives in mouth and pelvis (instead of gut like bac.)
  3. it has no dismutase so is less tolerant of oxygen
  4. not encapsulated
  5. doesn’t get into bloodstream
234
Q

Although it is an anaerobe, how are bacterioles able to survive if exposed to oxygen?

A

They have an oxygen toleronce due to super oxide dismutase and catalase presence.

235
Q

Pathogenesis of Prevotella spp

A

Mixed abscess is formed

236
Q

What main Prevotella spp are associated with female genital tract infections? With oral/GU/GI tract infections?

A

Genital tract infections: P. bivia; P. disiens

Oral/GU/GI: P. melaninogenica

237
Q

What are the 2 main types of Fusobacterium and what are their key clinical features?

A
  1. F. nucleatum​: spiration pneumonia and other lung diseases, brain and liver abscess, otitis media and sinusitis
  2. F. necrophorum​: Lemierre’s syndrome (bacterial infection coasues abscess which leads to clot formation, embolis and sepsis); highly virulent (potent endotoxin)
238
Q

Bacteroides are all resistant to what drug…

Which is why you must…

A

Penicillin

Must co-administer if penicillin family member is given (example ampicillin/ sulbactam)

239
Q

The 3 main types of chlamydiaceae

A

Chlamydia (1. C. trachomatis)

Chlamydophila (2. C. psittaci; 3. C. pneumoniae)

240
Q

Is Chlamydia intracellular or extracellular? Why? How does this play a role in its pathogenesis?

A

It is an obligate intracellular bacteria because it depends on the host cell for ATP.

The actual disease of chlamydia is based on it passing from cell to cell as elementary bodies that fill the cell until lysing and then pass onto other cells (causing inflammation)

241
Q

A/B/C Immunotypes of C. trachomatis

A

Trachoma

Prevalent worldwide and causes follicular conjunctivitis, eyelid curling and scaring which leads to blindness. Major cause of blindness worldwide.

242
Q

D-K serotypes of C. trachomatis

A

Common STD form

Leads to urethritis in males but is relatively asymptomatic for women (maybe cervicitis) which is why in can often lead to ovarian scarring and infertility.

243
Q

What effects can serotype D-K of C. trachomatis have on neonates?

A

Chlamydia that the mom has can lead to infant pneumonia or neonatal conjunctivitis

244
Q

L1,2,3 serotype of Chlamydia trachomatis info and clinical manifestations

A

Lymphogranuloma venereum

Often found in South America and Africa. Suppurative multilocular inguinal lymph nodes (bubos)

245
Q

Main method of diagnosis for Chlamydia trachomatis. What doesn’t this work for?

A

DNA probe of ribosomal RNA

Doesn’t work will for LGV (serology is used)

246
Q

Treatment of Chlamydia trachomatis

A

Penicillin is not effective because of a lack of peptidoglycan for chlamydia species.

Other anti-biotics are given usually for 7 days (tetracyclines, quinolones, erythromycin); Azithromycin is a one and done dose.

This works for everything but Lymphogranuloma which requires a 3 week course.

247
Q

What is missing from Chlamydia’s cell wall?

A

NO PEPTIDOGLYCANS!!!

248
Q

Cliical manifestations of C. pneumoniae

A

Can be pharyngitis, laryngitis or a walking pneumonia

249
Q

Clinical Manifestation and Pathogenesis of C. psittaci

A

Caused by inhalation of respiratory secretions or droppings of infected birds (usually exotic birds)

Leads to lower respiratory infection

250
Q

Pathogenesis of mycoplasm pneumoniae

A

Attaches to clilia/ microvilli of bronchial epithelium and causes inflammatory response which can lead to walking pneumonia

251
Q

Epidemiology of Mycoplasma pneumoniae

A
  • Epidemics every 4-7 years
  • Usually originates in young people and spreads among families
  • One person is infected and just as they feel better someone else shows symptoms (due to incubation period)
252
Q

Staining of Legionella

A

Technically gram-negative but does not stain well. Requires silver stain to be visible.

253
Q

What is the most common Legionella serotype?

A

Serotype 1

254
Q

What is the key cultural characteristic of Legionella? How does this effect its treatment.

A

It is beta-lactamase positive so no penicillin drugs will be useful.

255
Q

Epidemiology of Legionella (where is it found? who does it effect most?)

A

Lives in water and is often in aquatic lakes or man-made reservoirs. Can be found in potable water systems because it survives in biofilms.

Often healthcare associated and specifcally has a heavier effect on unhealthy people (organ recipients, cigarette smokers, chronic lung disease)

256
Q

Pathogenesis of Legionella. What are the 2 main clinical manifestations?

A

It is inhaled and uses a porin to bind to complement receptors and become endocytosed so that it can multiply intracellular.

  1. ​Pontiac Fever- febrile influenza-like illness ​w/o​ respiratory component. Short incubation and self-limited.
  2. Legionellosis- very severe pneumonia​. Longer incubation and multilobar with ability to reach multiple systems
257
Q

Special media for culturing Legionella

A

Buffered charcoal yeast extract agar (BYCE)

258
Q

Test for diagnosis of Legionella

A

Urinary antigen test can be used specifically to test for the serogroup 1​ type of legionella (because this is most common). Not definitive because there are other serotypes.

259
Q

Main treatments for Legionella

A

Macrolides or Fluoroquinolones

260
Q

What are the 2 bacteria species that form spores

A
  1. Bacillus
  2. Clostridium
261
Q

4 major virulence factors for Enterobacteriaceae

A
  • Endotoxins
  • Capsule
  • Antigenic Phase Variation
  • Type IIIsecretion systems
262
Q

Treatment of Salmonella

A

Third Generation Cephalosporin

MHD I (3 decks)

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